Research

1. Immune Regulation of Cardiac Fibrosis

Our laboratory investigates how immune cells affect fibrotic remodeling in the heart following injury. We study the roles of neutrophils, monocytes/macrophages, and other immune populations in driving fibroblast activation, extracellular matrix deposition, and scar formation. Using advanced transcriptomic, in vivo and in vitro models and imaging approaches, we aim to identify immune-derived pathways that contribute to maladaptive fibrosis and uncover new targets for restoring balanced tissue repair.

2. Immune–Vascular Crosstalk in Cardiovascular Disease

We explore how immune cells communicate with vascular endothelial and smooth muscle cells during atherosclerosis, myocardial infarction, and vascular inflammation. Our research focuses on adhesion molecules, chemotactic cues, metabolic signals, oxidative pathways and signaling mechanisms that regulate leukocyte recruitment, endothelial dysfunction, and vascular remodeling. By mapping these interactions, we seek therapeutic strategies that modulate immune–vascular signaling to preserve vascular health.

3. Neutrophils, NETosis, and Fibroblast Activation

This research theme examines how neutrophils and NET formation influence fibroblast behavior during cardiac remodeling. We study how NET components affect fibroblast proliferation, differentiation into myofibroblasts, and production of extracellular matrix proteins. Through in vitro and in vivo models, we aim to define the molecular pathways through which NETs trigger pathological tissue stiffening and evaluate whether targeting these mechanisms can limit cardiac fibrosis.

4. Monocyte–Endothelial Interactions in Diabetic Aortic Valve Disease

Our team investigates how diabetes modifies communication between circulating monocyte subsets and aortic valve endothelial cells. We study how hyperglycemia, oxidative stress, and inflammation reshape endothelial function and promote pro-calcific signaling. By characterizing monocyte-driven endothelial activation and endothelial-to-mesenchymal transition, we aim to uncover diabetes-specific mechanisms that accelerate valvular fibrosis and calcification.

5. miR-210 in Monocyte and Macrophage Function After Myocardial Infarction

We investigate the role of miR-210 in regulating monocyte and macrophage responses within the infarcted heart. Our work focuses on how miR-210 influences macrophage polarization, hypoxia adaptation and cytokine release during post-infarction healing. Through functional modeling and molecular profiling, we aim to determine whether miR-210–based interventions can enhance inflammation resolution and improve cardiac repair.